Having shown an increase in basic FGF immunoreactivity of the myocardium that becomes necrotic over the hour following excision of the heart, we sought to determine what aspects of the ischemic and/or necrotic process accounted for this increased immunoreactivity. Because it seemed unlikely that basic FGF could be synthesized in such a short time and because we and others have shown that basic FGF is present in extracellular matrix and that FGF can be extracted with acid, we hypothesized that the acidosis of ischemia might release basic FGF from extracellular matrix and prevent the binding of intracellular stores of FGF to matrix on lysis of these cells. We found that acidosis to the extreme limits of that found in necrotic tissue was able to reproduce the effects of the ischemia itself which we take to be partial evidence in support of the hypothesis.